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IntroductionEarly hemorrhage is often missed by traditional vital signs because of physiological reserve, especially in the young and healthy. We have developed a novel, wearable, wireless Doppler ultrasound patch that tracks real-time blood velocity in the common carotid artery.Materials and MethodsWe studied eight healthy volunteers who decreased their cardiac output using a standardized Valsalva maneuver. In all eight, we simultaneously monitored the velocity time integral (VTI) of the common carotid artery (using the ultrasound patch) as well as the descending aorta (using a traditional pulsed wave duplex imaging system); the descending aortic VTI was used as a surrogate for left ventricular stroke volume (SV). Additionally, in a subset of four, we simultaneously measured SV using a noninvasive pulse contour analysis device.ResultsFrom baseline to peak effect of Valsalva, there was a statistically significant fall in descending aortic and common carotid VTI of 37% (P = 0.0005) and 23% (P ConclusionIn summary, a novel index from a wireless Doppler ultrasound patch may be more sensitive and specific for detecting decreased cardiac output than standard vital signs in healthy volunteers.

No previous study has investigated the predictive risk factors of the nursing diagnosis of risk for decreased cardiac output after coronary artery bypass grafting (CABG).This study aimed to identify the predictive risk factors of the nursing diagnosis of risk for decreased cardiac output after CABG.This was a prospective cohort study performed at a cardiac university hospital in São Paulo, Brazil and 257 adult patients undergoing CABG were included. Potential risk factors for low cardiac output in the immediate post-operative period were investigated using the patients' medical records. Univariate analysis and logistic regression were used to identify the predictive risk factors of decreased cardiac output. The area under the receiver operating characteristic curve was calculated as a measure of accuracy. The variables that could not be analysed through logistic regression were analysed through Fisher's exact test.One hundred and ninety-five patients had low cardiac output in the immediate post-operative period. The predictive risk factors included age ⩾60 years, decreased left ventricle ejection fraction, not using the radial artery graft, positive fluid balance and post-operative arrhythmia that differed from the pre-operative arrhythmia. This model predicted the outcome with a sensitivity of 62.9%, a specificity of 87.2% and an accuracy of 81.5%. The variables analysed through Fisher's exact test included heart failure, re-exploration and bleeding-related re-exploration.The predictive risk factors for the nursing diagnosis of risk for decreased cardiac output after CABG were found. These results can be used to direct nurses in patient monitoring, staff training and nursing team staffing.

The development of acute kidney injury in patients with pulmonary embolism (PE) has not been well documented. We report a patient who developed acute oliguria in the setting of massive PE. Catheter embolectomy followed by ultrafiltration resulted in an immediate and dramatic improvement in urine output. Uncharacteristically, serum creatinine did not rise during the oliguric phase for several days until after embolectomy, and there were no metabolic derangements. Our observation that embolectomy and ultrafiltration helped with hemodynamics and renal perfusion despite decreased cardiac output suggests that right ventricular failure from both pressure and volume overload may have been central to this process. We review the older and recent literature in support of our observations.

Heart failure (HF) is a common disease associated with poor prognosis. Anaemia is commonly associated with HF due to bone marrow depression, reduced availability of iron and haemodilution, and is sometimes aggravated by too frequent blood testing. Low haemoglobin is very detrimental to the haemodynamic state of the patient with decreased cardiac output as it further diminishes the oxygen supply to the tissues. When anaemia is associated with HF. and renal failure, the patient enters a vicious cycle called cardio renal anaemia syndrome. The prognosis of patients with HF is worse as the haemoglobin is lower and even mild anaemia is associated with

See article by Takahashi et al. (pages 356–365) in this issue . Despite major progress in the pharmacological management of congestive heart failure (CHF), life expectancy of patients suffering from CHF remains low [1]. Progress in the treatment of CHF (currently based on diuretics, angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II (Ang II) type 1 receptor (AT1R) blockers (ARB), and β-blockers [1]) has relied on the recognition of the primary role of the adrenergic and renin–angiotensin–aldosterone (RAA) systems, which are initially activated to compensate for the decreased cardiac output, but which, in the long run, aggravate myocardial performance, therefore perpetuating the vicious circle of the CHF process [2]. The myocardium is one final target of the deleterious effects of catecholamines and Ang II. This has led to the carrying out of studies aimed at understanding the damage done to cardiac myocytes and the potential beneficial effects of molecules protecting, directly or indirectly (through haemodynamic changes), the myocardium. Such studies at the myocyte level are still rare and mostly conducted in animal models of CHF [3]. Despite the variety of CHF models, major convergent findings have been disclosed. These include modified expression or activity of proteins involved in the excitation–contraction–coupling process and its neurohormonal modulation: ion channels (voltage-activated potassium channels), transduction pathway components (such as decreased expression of β1-adrenergic receptors, increased expression of Gi protein), intracellular calcium-regulating proteins (decreased expression of sarcoplasmic reticulum calcium ATPase, increased expression of the sarcolemmal Na/Ca exchanger, altered function of the … *Tel.: +33 2 41 22 8269; fax: +33 2 41 8228. Email address: stephane.baudet{at}intervet.com

Objective: The aim was to evaluate the effect of hypertonic perfusate on isolated left ventricular mechanical and energetic characteristics. Methods: An isolated working rat heart model was perfused with a hyponatraemic Krebs-Heinseleit bicarbonate buffer (240 mOsmol·litre−1). To this buffer was added increasing amounts of mannitol to achieve 280, 320, and 360 mOsmol·litre−1 perfusates. Results: Left ventricular peak pressure, maximum time derivative of left ventricular pressure (dP/dtmax), and end systolic pressure were all increased to a maximum value at 280 or 320 mOsmol·litre−1 perfusate tonicity. A similar response was evident with cardiac output, which changed from 33.7(SEM 0.6) to 43.5(0.8) ml·min−1 following changing the perfusate tonicity from 240 to 280 mOsmol·litre−1 (p≤0.003). However, increasing perfusate tonicity further decreased cardiac output to 36.5(1.3) ml·min−1 at 360 mOsmol·litre−1. Maximal left ventricular elastance remained unchanged during perfusion with increasing perfusate tonicities. Conclusions: Changing perfusate osmolality using mannitol has a positive inotropic effect at low osmolalities and a negative inotropic effect at perfusate osmolality greater than 320 mOsm·litre−1.

Atrial fibrillation (AF) is the most common tachyarrhythmia in humans. It causes palpitations, decreased cardiac output, heart failure and systemic thromboembolism, and is associated with significant morbidity, mortality1 and healthcare costs. Current treatment strategies for AF are far from satisfactory. Atrial fibrillation has a tendency to become more persistent with time, a large percentage of patients with paroxysmal AF eventually developing chronic AF.2 Although progression of an underlying disease has previously been considered as the most likely explanation for this phenomenon, in a proportion of cases, no underlying disease is evident. Recently Wijffels and coworkers have demonstrated, in a chronically instrumented conscious goat model, that episodes of AF may be self‐perpetuating (‘AF begets AF’) and have suggested that there may be a purely electrophysiological explanation (termed atrial electrical remodelling) for the increased persistence of AF with time.3 This hypothesis has considerable clinical importance in that it would, if proven, support a more aggressive approach to the overall management of AF. If AF leads to more AF, then it is reasonable to expect that earlier termination and preventative therapy for the arrhythmia would improve the long‐term outcome of patients with the condition. In the original model of Wijffels and Allessie,3 goats initially had electrodes sutured to the epicardium of both atria. After this initial surgery, the goats were connected to an external automatic fibrillator. The device was programmed to deliver a 1 s burst of electrical stimuli whenever sinus rhythm was sensed. In the normal animal, the first …

The effects of endothelin on systemic hemodynamics and renal functions were investigated in anesthetized dogs. Infusion of endothelin at a dose of 1 ng/kg/min decreased renal blood flow and increased renal vascular resistance and filtration fraction. Endothelin at doses higher than 10 ng/kg/min significantly decreased cardiac output, glomerular filtration rate, renal plasma flow, urine volume, and urinary sodium excretion. Mean arterial pressure showed a transient decrease at doses higher than 50 ng/kg/min. These results showed that endothelin in systemic administration has effects on renal functions as well as on systemic hemodynamics.

To investigate the possibility that seasonal adaptation requires significant hemodynamic changes, 5 normotensive and 21 mildly hypertensive subjects were followed through 4 seasons for changes in systemic hemodynamics and sympathetic nervous activity. In the upright position wintertime blood pressures increased by 3% (P = NS) over summer values whereas cardiac output and stroke volume decreased by 18% and 21%, respectively (P less than .0017 for each). Similarly, wintertime upright heart rate increased by 7% (P less than .017) with larger parallel increases in systemic vascular resistance (+24%, P less than .0017) and plasma norepinephrine (+26%, P less than .017). The supine values followed similar trends but the magnitude of changes was about 50% less than the corresponding upright values. Thus, in the northern US, wintertime vasoconstriction is related to increased sympathetic nervous activity and decreased cardiac output. When these reciprocal changes are proportional, blood pressure remains constant.

Elderly surgical patients are especially susceptible to incidental hypothermia. Thermoregulatory mechanisms and cardiopulmonary systems are limited in recovery potential. To prevent postoperative shock secondary to decreased cardiac output an hypoxia, temperature should be carefully monitored with vital signs during and after surgery.